Monday, 23 April 2012

Genetics of ADHD

Michael Wyld – s4290703

Genetics: The key to understanding disease

Could you imagine a world with no disease? A world with absolutely no sickness, mental or physical? Impossible, you might say, being sick is just comes with being alive! What could possible halt the massive array of diseases which we are subject to? One word: genetics.  By identifying and understanding the genes involved in causing illnesses, prevention and treatment become possible, and you’ll never be able to use the sickness excuse to get off work again!

Unfortunately, it’s very difficult to pinpoint the exact genes involved in causing certain diseases. In particular, genomics, the study of genomes in organisms, has had little impact to date on psychiatric disorders such as attention deficit hyperactivity disorder (ADHD) (Ross 2012). Recent articles in this area have provided significant insight into the causation of ADHD, however. These findings may open the path for future research into ADHD and other psychiatric disorders, possibly even leading to finding a cure in the future!

ADHD, CNVs and the disease hypotheses

Figure 1: A bran scan of the brains of a
non- ADHD control and an ADHD
For both children and adults, attention deficit hyperactivity disorder (ADHD) is one of the most widespread neuropsychiatric disorders (Williams et. al. 2012). It is easily passed on from parent to child and is caused by both genetic and environmental influences. Recent articles have used an alternative hypothesis to previous studies called the multiple rare variant framework, which proposes the cause of common diseases as the result of rare variants in the genetic code (Ross 2012). This model uses the identification of copy number variants (CNVs) in order to look at genetic causes for diseases. In every person’s genetic code, there will be large deletions or duplications covering one or more genes, which are these CNVs (Ross 2012). By analyzing the differences between CNVs in healthy and unhealthy genetic code, we try to determine which genes are involved in diseases.

But how can this link to the causes of ADHD?

In a recent article, Williams et. al. (2012) used this method to study CNVs in a sample of young people with ADHD compared to a sample without ADHD. These geneticists found that the ADHD group contained 1.15 times as many CNVs as the healthy control group, in particular in areas which had already been linked to autism and schizophrenia (Ross 2012). In another study conducted by Elia et. al. (2012), 12 sites of greater CNV numbers in an ADHD group compared to a healthy group were found, along with over 200 genes which were influenced by specific CNVs found in the study. These findings suggested that future studies could in fact point towards clinical research into potential ADHD treatment.
Figure 2: A complex map of the gene networks influenced by ADHD (Elia et. al. 2012)

Where to from here?

As research in this area continues, we will see a greater and greater understanding of the genetic causes for ADHD, and using this framework, perhaps a greater understanding of other psychiatric disorders too. In the future we might even see new, more effective treatments for ADHD emerging, possibly leading into a permanent cure. With the constant advance of genetics, a disease-free world is becoming closer and closer to reality!

Reference List:
  • Elia, J, Glessner, J, Wang, K, Takahashi, N, Shtir, C, Hadley, D, Sleiman, P, Zhang, H, Kim, C, Robison, R, Lyon, G, Flory, J, Bradfield, J, Imielinski, M, Hou, C, Frackelton, E, Chiavacci, R, Sakurai, T, Rabin, C, Middleton, F, Thomas, K, Garris, M, Mentch, F, Freitag, C, Steinhausen, C, Todorov, A, Reif, A, Rothenberger, A, Franke, B, Mick, E, Roeyers, H, Buitelaar, J, Lesch, K, Banaschewski, T, Ebstein, R, Mulas, F, Oades, R, Sergeant, J, Sonuga-Barke, E, Renner, T, Romanos, M, Romanos, J, Warnke, A, Walitza, S, Meyer, J, Pálmason, H, Seitz, C, Loo, S, Smalley, S, Biederman, J, Kent, L, Asherson, P, Anney, R, Gaynor, J, Shaw, P, Devoto, M, White, P, Grant, S, Buxbaum, J, Rapoport, J, Williams, N, Nelson, S, Faraone, S & Hakonarson, H, 2012, ‘Genome-wide copy number variation study associates metabotropic glutamate receptor gene networks with attention deficit hyperactivity disorder’, Nature Genetics, vol.44, no. 1, viewed 15 March 2012, <>.
·         Ross, RG 2012, ‘Advances in the Genetics of ADHD’, American Journal of Psychiatry, vol. 169, no. 2, viewed 13 March 2012, <>.

·         Williams, N, Franke, B, Mick, E, Anney, R, Freitag, C, Gill, M, Thapar, A, O’Donovan, M, Owen, M, Holmans, P, Kent, L, Middleton, F, Zhang-James, Y, Liu,L, Meyer, J, Nguyen, T, Romanos, J, Romanos, M, Seitz, C, Renner, T, Walitza, S, Warnke, A, Palmason, H, Buitelaar, J, Rommelse, N, Vasquez, A, Hawi, Z, Langley, K, Sergeant, J, Steinhausen, H, Roeyers, H, Biederman, J, Zaharieva, I, Hakonarson, H, Elia, J, Lionel, A, Crosbie, J, Marshall, C, Schachar, R, Scherer, S, Todorov, A, Smalley, S, Loo, S, Nelson, S, Shtir, C, Asherson, P, Reif, A, Lesch, K &Faraone, S 2012, ‘Genome-wide analysis of copy number variants in attention deficit hyperactivity disorder: the role of rare variants and duplications at 15q13.3’, American Journal of Psychiatry, vol. 169, no. 2, pp. 195-204.

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